1994 Fiscal Year Final Research Report Summary
Role of Calcium Signaling Pathway for Cardiac Cell Injury
| Project/Area Number |
05304033
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
TADA Michihiko Osaka Univ., Medical School., Professor, 医学部, 教授 (90093434)
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| Co-Investigator(Kenkyū-buntansha) |
ENDO Masao Yamagata Univ., Medical School., Professor, 医学部, 教授 (40004668)
TSUKITA Shoichiro Kyoto Univ., Medical School., Professor, 医学部, 教授 (50155347)
TOYAMA Junji Nagoya Univ., Inst.of Enviomment Medicine., Prof., 環境医学研究所, 教授 (20023658)
HORI Masatsugu Osaka Univ., Medical School., Associate Prof., 医学部, 講師 (20124779)
KUZUYA Tsunehiko Osaka Univ., Medical School., Associate Prof., 医学部, 助教授 (80150340)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Adhesion molecule / Calcium signaling / Myocardial injury / Reperfusion / Heart failure / Low molecuar weight G-protein / Intercalated disc / Gap junction |
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| Research Abstract |
In cardiac muscle, calcium plays a key role in excitation-contraction coupling. In this study, we investigated contribution of the proteins mediating excitation-contraction coupling for myocardial injury.
We identified the interaction sites in phospholamban and the Ca ATPase molecule by using molecular biological methods. We investigated gene regulation of phospholamban and the Ca ATPase, indicating thyroid hormone is a key foactor for the regulation of those gene expression. Regulator binding domain was identified in the Ca release channel of the cardiac sarcoplasmic reticulum. Electrophysiological study on gap junction showed that the activity of gap junction is regulated by calmodulin. We purified and determined the primary structure of adherens junction proteins. We showed that a low molecular weight G-protein, rho regulates cell shape and mobility via actomyosin system.
Calcium overload is a dominating factor for reperfusion injury of myocardium. This might mediated by Ca-dependent proteinase.
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